Binge eating is a behavior that is characteristic of a variety of eating and weight problems, and a fundamental question persists in clinical work as to what drives binge eating episodes. Situational increases in negative affect have been linked to occurrence of binge eating; however, the neural and behavioral mechanisms by which such increases in negative affect may make binge eating more likely to occur have not been extensively investigated. This R21 proposal seeks to develop novel methods that will examine (behaviorally and neurally) how emotions impact impulsivity in patients who binge eat, by developing a novel functional magnetic resonance imaging (fMRI) affect induction paradigm. This proposal is to develop methods that can eventually be applied to a variety of eating problems and behaviors. This proposal initiates these methods with the study of patients with bulimia nervosa (BN), a population representing the most pathological end of the binge eating spectrum. We will study how emotions impact impulsivity in BN as measured by an fMRI impulse control task, performed at baseline and under conditions of both negative and positive affect induction. If this approach proves useful, the methods developed can be extended to other presentations of binge- and over- eating, consistent with the RDoC approach. In the proposed affect induction paradigm, sustained negative affect will be induced using a psychophysiologically validated manipulation of an unpredictable threat (burst of white noise) occurring during discrete intervals of the task and not during other intervals. To control for general arousal effects of this negative affect manipulation, we will also induce sustained positive affect whereby an unpredictable positive event (chance of winning up to $100) may occur. For the study of impulse control, we propose to use two go/nogo tasks as neurocognitive probes - a food variant and a non-food, emotional variant. Hypotheses include: (1) behaviorally, in BN, negative affect induction will downregulate impulse control, as demonstrated by more false alarms during the induced negative affect condition, relative to control subjects (2) patient with BN will demonstrate lower BOLD signal in inhibitory control (e.g. inferior frontal cortex) and emotion regulation regions (ventromedial PFC) during induction of negative affect, and increased BOLD signal when attempting to suppress responding to appetitive cues embedded in the food-related task. Such results would demonstrate a mechanism through which negative affect interacts with brain circuitry mediating impulse control. Results from the development of these methods may lend themselves to larger studies, in which these probes of impulse control in the face of sustained negative or positive affect may be tested across a variety of syndromal and subsyndromal eating problems and behaviors, and may support future treatment development which focuses on the link between emotion regulation and impulsivity.